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Apoa-I Deficiency Increases Cortical Amyloid Deposition, Cerebral Amyloid Angiopathy, Cortical And Hippocampal Astrogliosis, And Amyloid-Associated Astrocyte Reactivity In App/Ps1 Mice, Emily B. Button, Guilaine K. Boyce, Anna Wilkinson, Sophie Stukas, Arooj Hayat, Jianjia Fan, Brennan J. Wadsworth, Jerome Robert, Kris M. Martens, Cheryl L. Wellington
Apoa-I Deficiency Increases Cortical Amyloid Deposition, Cerebral Amyloid Angiopathy, Cortical And Hippocampal Astrogliosis, And Amyloid-Associated Astrocyte Reactivity In App/Ps1 Mice, Emily B. Button, Guilaine K. Boyce, Anna Wilkinson, Sophie Stukas, Arooj Hayat, Jianjia Fan, Brennan J. Wadsworth, Jerome Robert, Kris M. Martens, Cheryl L. Wellington
Faculty & Staff Scholarship
Background
Alzheimer’s disease (AD) is defined by amyloid beta (Aβ) plaques and neurofibrillary tangles and characterized by neurodegeneration and memory loss. The majority of AD patients also have Aβ deposition in cerebral vessels known as cerebral amyloid angiopathy (CAA), microhemorrhages, and vascular co-morbidities, suggesting that cerebrovascular dysfunction contributes to AD etiology. Promoting cerebrovascular resilience may therefore be a promising therapeutic or preventative strategy for AD. Plasma high-density lipoproteins (HDL) have several vasoprotective functions and are associated with reduced AD risk in some epidemiological studies and with reduced Aβ deposition and Aβ-induced inflammation in 3D engineered human cerebral vessels. In mice, …